| Autor: |
Mazzanti CM; Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcellos, 2600-Anexo, 90035-003 Porto Alegre, RS, Brazil., Spanevello R, Ahmed M, Schmatz R, Mazzanti A, Salbego FZ, Graça DL, Sallis ES, Morsch VM, Schetinger MR |
| Jazyk: |
angličtina |
| Zdroj: |
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience [Int J Dev Neurosci] 2007 Jun; Vol. 25 (4), pp. 259-64. Date of Electronic Publication: 2007 Mar 07. |
| DOI: |
10.1016/j.ijdevneu.2007.02.005 |
| Abstrakt: |
Cyclosporine A is the major immunosuppressive agent used for organ transplantation and for the treatment of a variety of autoimmune disorders such as multiple sclerosis. In this work, we investigated the effect of the cyclosporine A on the acetylcholinesterase activity in the cerebral cortex, striatum, hippocampus, hypothalamus, cerebellum and pons of the rats experimentally demyelinated by ethidium bromide. Rats were divided into four groups: I control (injected with saline), II (treated with cyclosporine A), III (injected with 0.1% ethidium bromide) and IV (injected with 0.1% the ethidium bromide and treated with cyclosporine A). The results showed a significant inhibition (p<0.05) of acetylcholinesterase activity in the groups II, III and IV in all brain structures analyzed. In the striatum, hippocampus, hypothalamus and pons the inhibition was greater (p<0.005) when ethidium bromide was associated with cyclosporine A. In conclusion, the present investigation demonstrated that cyclosporine A is an inhibitor of acetylcholinesterase activity and this effect is increased after an event of toxic demyelination of the central nervous system. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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